Journal
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
Volume 324, Issue 2, Pages 810-814Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.bbrc.2004.08.238
Keywords
peroxisome proliferator-activated receptor-gamma; pancreatic beta-cells; insulin secretion; pancreatic alpha-cells; glucagon secretion; uncoupling protein-2
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Peroxisome proliferator-activated receptor-gamma (PPAR-gamma) regulates several cellular functions, but its physiological role in pancreatic islet cells remains to be investigated. In this study, we confirmed the presence of PPAR-y in rat isolated islets and examined its role on insulin and glucagon secretion by using PPAR-gamma-overex pressed islets. PPAR-y overexpression significantly suppressed insulin secretion induced by stimulatory concentration of glucose (p < 0.05). In addition, insulin secretion evoked by high potassium depolarization also was significantly decreased from PPAR-gamma-overexpressed islets (p < 0.05). On the other hand, no significant change in glucagon release was observed after high potassium depolarization between PPAR-gamma-overexpressed and control islets. Insulin and glucagon content in islets was not statistically different between the two groups. In addition, the expression of uncoupling protein-2 (UCP-2) was found to be induced in PPAR-gamma-overexpressed islets. This result clearly indicates that the deteriorative effect of PPAR-gamma overexpression on the secretory machinery is selective for pancreatic beta-cells. And it is possible that its site of action can be located in the energy-consuming exocytotic process of insulin secretory granules, and that the reduction of ATP production through increased UCP-2 reduces insulin exocytosis. (C) 2004 Elsevier Inc. All rights reserved.
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